A Discussion of Electrochemical Techniques for the Detection of Nitric Oxide

Wink, David A.; Christodoulou, Danae; Ho, May Y. K.; Krishna, Murali C.; Cook, John A.; Haut, Harold; Randolph, J.Kemp; Sullivan, Margery; Coia, George M.; Murray, Royce R.; Meyer, Thomas

doi:10.1006/meth.1995.1010

Cited by 52 publications

(41 citation statements)

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“…In addition, the coating polymer used for the recording electrode provides very adequate anion exclusion, particularly of amino acids, such that contamination by glutamate or aspartate is unlikely [20]. Finally, although interference by high dopamine concentrations is possible [17], we did not find evidence for changes in NO electrochemical detection at both extremes of oxygen concentration within the calibration solutions. The present data further concur with a recent report by Rivot et al [21] who showed that continuous NO production occurs within the nervous tissue, is enhanced by NMDA, and can be modified by NOS inhibitors and NO donors.…”

Section: Discussioncontrasting

confidence: 35%

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Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Gozal

Torres²

2001

Neonatology

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Gasping is an important mechanism for survival that appears to be developmentally modulated by the glutamate-nitric oxide (NO) pathway. However, the temporal characteristics of NO brain tissue levels during gasping are unknown. We hypothesized that during anoxia-induced gasping, the gasping frequency would be closely correlated with caudal brainstem tissue NO concentrations in developing rats. Brainstem and cortical tissue NO levels were measured during anoxia using a voltammetric electrode in adult rats and 5-day-old pups during control conditions and following pretreatment with the NMDA receptor antagonist MK-801 (1 mg/kg) or the neuronal NO synthase inhibitor 7-nitro-indazole (7-NI; 100 mg/kg). In young animals, NO tissue levels followed a triphasic trajectory coincident with gasp frequency which was markedly altered by MK-801 and 7-NI, albeit with preservation of gasp frequency-NO tissue level relationships. In adult rats, 40-fold higher NO tissue levels occurred and followed a monophasic trajectory coincident with gasp patterning. In the cortex, monophasic increases in NO levels occurred at all ages. We conclude that anoxia-induced gasping neurogenesis is modulated via NMDA-NO mechanisms in the developing rat. We postulate that higher NO brainstem concentrations may favor early autoresuscitation, but limit anoxic tolerance.

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Section: Discussioncontrasting

confidence: 35%

“…In vivo voltammetric measurements of NO using coated carbon fiber microelectrodes have been previously validated by various investigators [16][17][18][19]. Such studies have also shown that neither MK-801 nor 7-NI administration interferes with in vivo brain tissue NO measurements.…”

Section: Discussionmentioning

confidence: 96%

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Gozal

Torres²

2001

Neonatology

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“…Methods for electrochemical detection of NO have recently become available (Wink et al, 1995;Christodoulou et al, 1996;Allen et al, 2000;Brunet et al, 2003;Zhang, 2004;Nunemaker et al, 2007), enabling measurements of NO on the second and sub-second time scales in local regions of neural circuitry in vivo (Buerk et al, 1996;Buerk et al, 2003a;Buerk et al, 2003b), in brain slices in vitro (Leonard et al, 2001;Ledo et al, 2002;Ferreira et al, 2005) and in neuronal cell cultures (Oni et al, 2004;Xu et al, 2004;Pereira-Rodriques et al, 2005). Here, we show for the first time that NO-selective microelectrodes can be used to measure NO production in the living mouse olfactory bulb.…”

Section: Introductionmentioning

confidence: 83%

Tonic and stimulus-evoked nitric oxide production in the mouse olfactory bulb

Lowe

Buerk

et al. 2008

Neuroscience

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Nitric oxide (NO) has been long assumed to play a key role in mammalian olfaction. This was based largely on circumstantial evidence, i.e. prominent staining for nitric oxide synthase (NOS) and cyclic GMP or soluble guanylyl cyclase, an effector enzyme activated by NO, in local interneurons of the olfactory bulb. Here we employ innovative custom-fabricated NO micro-sensors to obtain the first direct, time-resolved measurements of NO signaling in the olfactory bulb. In 400 μm thick mouse olfactory bulb slices, we detected a steady average basal level of 87 nM NO in the extracellular space of mitral or granule cell layers. This NO 'tone' was sensitive to NOS substrate manipulation (200 μM L-arginine, 2 mM L-NAME) and Mg 2+ modulation of NMDA receptor conductance. Electrical stimulation of olfactory nerve fibers evoked transient (peak at 10 s) increments in NO levels 90 -100 nM above baseline. In the anesthetized mouse, NO micro-sensors inserted into the granule cell layer detected NO transients averaging 55 nM in amplitude and peaking at 3.4 sec after onset of a 5 sec odorant stimulation. These findings suggest dual roles for NO signaling in the olfactory bulbtonic inhibitory control of principal neurons, and regulation of circuit dynamics during odor information processing.

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“…Control is quite stable and has a sensitivity range of 100 nm NO as previously reported Wink et al, 1995a). and DEA/NO treated cells were sampled during and after DEAINO treatment.…”

Section: Glutathione (Gsh) Measurementsmentioning

confidence: 90%

Nitric oxide enhancement of melphalan-induced cytotoxicity

Cook

Krishna²,

Pacelli³

et al. 1997

Br J Cancer

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Summary The effects of the diatomic radical, nitric oxide (NO), on melphalan-induced cytotoxicity in Chinese hamster V79 and human MCF-7 breast cancer cells were studied using clonogenic assays. NO delivered by the NO-releasing agent (C2H5)2N[N(O)NO]-Na+ (DEA/NO; 1 mM) resulted in enhancement of melphalan-mediated toxicity in Chinese hamster V79 lung fibroblasts and human breast cancer (MCF-7) cells by 3.6-and 4.3-fold, respectively, at the IC50 level. Nitrite/nitrate and diethylamine, the ultimate end products of DEANNO decomposition, had little effect on melphalan cytotoxicity, which suggests that NO was responsible for the sensitization. Whereas maximal sensitization of melphalan cytotoxicity by DEA/NO was observed for simultaneous exposure of DEA/NO and melphalan, cells pretreated with DEA/NO were sensitized to melphalan for several hours after NO exposure. Reversing the order of treatment also resulted in a time-dependent enhancement in melphalan cytotoxicity. To explore possible mechanisms of NO enhancement of melphalan cytotoxicity, the effects of DEANO on three factors that might influence melphalan toxicity were examined, namely NO-mediated cell cycle perturbations, intracellular glutathione (GSH) levels and melphalan uptake. NO pretreatment resulted in a delayed entry into S phase and a G/M block for both V79 and MCF-7 cells; however, cell cycle redistribution for V79 cells occurred after the cells returned to a level of cell survival, consistent with treatment with melphalan alone. After 15 min exposure of V79 cells to DEA/NO (1 mM), GSH levels were reduced to 40% of control values; however, GSH levels recovered fully after 1 h and were elevated 2 h after DEA/NO incubation. In contrast, DEANO (1 mM) incubation did not reduce GSH levels significantly in MCF-7 cells (approximately 10%). Melphalan uptake was increased by 33% after DEANNO exposure in V79 cells. From these results enhancement of melphalan cytotoxicity mediated by NO appears to be complex and may involve several pathways, including possibly alteration of the repair of melphalan-induced lesions. Our observations may give insights for improving tumour kill with melphalan using either exogenous or possibly endogenous sources of NO.Melphalan is a widely used chemotherapeutic agent for a variety of tumour types and is thought to exert its cytotoxic effect by alkylating and cross-linking DNA (Calabresi and Parks, 1985;Colvin and Chabner, 1990). Although melphalan has shown efficacy alone or in combination with other chemotherapeutic agents, there remains a need to explore avenues to broaden its spectrum and effectiveness. Intracellular glutathione (GSH) levels have been shown to modulate melphalan cytotoxicity, and depletion of GSH by buthionine sulphoximine (BSO) has been shown to enhance melphalan cytotoxicity significantly (Green et al, 1984;Ozols et al, 1987). Based on these preclinical findings, phase I clinical trials have been completed recently establishing a safe BSO dose to use in conjunction with melphalan (O'Dwyer et al, 1996).We have...

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A Discussion of Electrochemical Techniques for the Detection of Nitric Oxide

Cited by 52 publications

References 0 publications

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Brainstem Nitric Oxide Tissue Levels Correlate with Anoxia-Induced Gasping Activity in the Developing Rat

Tonic and stimulus-evoked nitric oxide production in the mouse olfactory bulb

Nitric oxide enhancement of melphalan-induced cytotoxicity

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